Rosa Aras-López

Pregnancy induces a number of immunological, hormonal, and metabolic changes that are necessary for the mother to adapt her body to this new physiological situation. The microbiome of the mother, the placenta and the fetus influence the fetus growth and undoubtedly plays a major role in the adequate development of the newborn infant. Hence, the microbiome modulates the inflammatory mechanisms related to physiological and pathological processes that are involved in the perinatal progress through different mechanisms. The present review summarizes the actual knowledge related to physiological changes in the microbiota occurring in the mother, the fetus, and the child, both during neonatal period and beyond. In addition, we approach some specific pathological situations during the perinatal periods, as well as the influence of the type of delivery and feeding.

To evaluate if the redox system is unbalanced in the hearts of nitrofen-induced congenital diaphragmatic hernia (CDH) animals and to study the possible preventive effects of two anti-oxidant treatments, apocynin and epigallocatechin-3-gallate (EGCG).

Metabolic reprogramming is a hallmark of cancer. We and other authors have previously shown that breast cancer subtypes present metabolism differences. In this study, breast cancer cell lines were treated with metformin and rapamycin. The response was heterogeneous across various breast cancer cells, leading to cell cycle disruption in specific conditions. The molecular effects of these treatments were characterized using sublethal doses, SNP genotyping and mass spectrometry-based proteomics. Protein expression was analyzed using probabilistic graphical models, showing that treatments elicit various responses in some biological processes, providing insights into cell responses to metabolism drugs. Moreover, a flux balance analysis approach using protein expression values was applied, showing that predicted growth rates were comparable with cell viability measurements and suggesting an increase in reactive oxygen species response enzymes due to metformin treatment. In addition, a method to assess flux differences in whole pathways was proposed. Our results show that these various approaches provide complementary information, which can be used to suggest hypotheses about the drugs’ mechanisms of action and the response to drugs that target metabolism.

Congenital diaphragmatic hernia (CDH) is one of the causes of respiratory failure in newborns due to lung hypoplasia and pulmonary abnormalities leading to pulmonary hypertension (PH). NAD(P)H oxidase (Nox) is a family of isoenzymes that generate reactive oxygen species (ROS) which can contribute to PH-induced vascular dysfunction. On the other hand, superoxide dismutase (SOD) 1–2 and catalase are the antioxidant enzymes that eliminate the excess of ROS in pulmonary vascular cells. Our aim is to examine whether PH-associated with CDH is due to a dysregulation of ROS production in lungs from CDH fetuses. Pregnant rats received either 100 mg nitrofen or vehicle on E9.5. Fetuses were recovered on E21. (1) Nox activity, (2) H₂O₂ production and (3) mRNA levels of Nox1, Nox2, Nox4, SOD1, SOD2 and catalase were analyzed in fetal lungs. Nox activity and Nox1 and Nox2 mRNA levels were increased in the lungs of fetuses with CDH. However, there were no changes in H₂O₂ production and Nox4 mRNA levels. SOD1, SOD2 and catalase were decreased. The raised oxidative stress due to increase in ROS generation by Nox isoenzymes and dysfunction of antioxidant enzymes seems to be a potential mechanism responsible on PH-associated with CDH.